BIOD65H3 Lecture : ALS Article #1 Notes

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Activated protein c therapy slows als-like disease in mice by transcriptionally inhibiting sod1 in motor neurons and microglia cells. present damage in: motor neurons, microglia, astrocytes, microvessel endothelium. study used: sod1 g93a, sod1 g85r, sod1g37r y par1: expressed in platelets, endothelium, certain neurons y epcr: it s through the epcr that apc is transported into the spinal cord isf. apc receptor found specifically in endothelial cells y sp1: transcirption factor regulates expression of genes involved in: cell growth, apoptosis, differentiation and immune responses y hypomorph: mutation that causes partial loss of gene function. Apc treatment delivered after disease onset controls progression of als-like disease: y als-linked mutant sod1 g93a mice put into one of the following groups: saline, wt-apc (active), 3k3a-apc (active), 5a-apc (active), s360a-apc (inactive) y given a low dose (40 g/kg/d i. p. ) or high dose: (100 g/kg/d i. p. ) of either saline or one of the apc analogs, 7 days after disease onset.

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